Trigeminal

neuralgia
Dr Priyanka
Consultant maxillofacial surgeon
Trigeminal Neuralgia
Contents:
1. Other names
2. Definition
3. Etiology
4. General characteristics
5. Clinical presentation
6. Clinical characteristics
7. Diagnosis
8. Treatment: medical and surgical
9. Post operative care.
 Trigeminal Neuralgia
Other names:
 Tic doloureux Nicholaus Andre
 Fothergill’s disease John Fothergill
 Neuralgia:Pain which follows the
path of specific nerves.

 Trigeminal Neuralgia: Is a facial pain

syndrome defined as sudden, usually
unilateral, severe, brief, stabbing,
lancinating, recurring pain in the
distribution of one or more branches
of the 5th cranial nerve and may be
elicited by touching trigger points in
the skin or the gums.
 Branches of trigeminal nerve:
 Ophthalmic

Frontal Nasiociliary Lacrimal

Long/ short Posterior Anterior Infra

Supraorbital supratrochlear
ciliary Ethmoidal Ethmoidal Trochlear
 maxillary

cranial PP fossa Infraorbital face

Middle Inferior
PP Nerve PASN Zygomatic MSAN
Meningeal Palpebral

Zygomatico-
orbital ASAN Nasal
Facial

Zygomatico- Superior
nasal Temporal Labial

palatine

Pharyngeal
 Mandibular

Main Trunk Anterior Posterior

M.Meningeal Buccal Massetric lingual

Nr. to Deep temporal

Nr. to
Auriculotemporal
medial Pterygoid Latral pterygoid

Inferior alveolar
 Etiology: The cause of this disease process is unknown.
 Vascular factors: Transient ischemia & autoimmune
hypersensitivity responses.
 Mechanical factors: anomaly of the superior cerebellar
artery has been more recently blamed for causing TN.
 Other Probable factors.
1. Dental etiology: According to westrum and black
differentiation from loss of the teeth& degeneration of the
nerve
2. Infections: Various granulomatous and non granulomatous
infections
 Rather’s jaw bone cavities: found in the alveolar & jaw bones.
 Multiple Sclerosis
 Petrous ridge (basilar) compression
 Post traumatic Neuralgia
  Intracranial tumors
 Intracranial vascular abnormalities
 Viral etiology

General Characteristics:
Incidence: It is a rare affliction, seen in about 4 in 100 000
people.
Age: middle age ( 5th to 6th Decade)
Sex: Female predilection ( 58% )
Affliction for side: Predilection for the right side is noted (
60% )
Division of trigeminal nerve involvement: V3 is more
involved than V2. Rarely involves V1.
Only sensory division is effected.
 Clinical presentation
 Sweet diagnostic criteria:
1. The pain is paroxysmal
2. The pain may be provoked by light touch to the face.
3. The pain is confined to the trigeminal distribution.
4. The pain is unilateral.
5. The clinical sensory examination is normal.
 White and sweet criteria for TN were a major
advance that facilitated research and enabled
early and accurate clinical recognition of the
syndrome. The criteria were incorporated, largely
unchanged, into the official research diagnostic
framework criteria published by the international
association for the study of pain and the
international headache socity.
 TN is further subdivided into classic and
systematic TN.
 Classic criteria:
1. Paroxysmal attacks of pain lasting from a
fraction of second to 2 min, affecting one or
more divisions of the trigeminal nerve and
fulfilling criteria 2 and 3.
2. Pain has any one of the characteristics.
1. Intense, sharp, superficial / stabbing
2. Precipitated from trigger area
3. Attacks are stereotyped in the individual
patient.
4. There is no clinically evident neurological
deficit.
5. Nor attributed to another disorder.
 Symptomatic criteria:
1. Paroxysmal attacks of pain lasting from a fraction of
a second to 2 min, with or without persistence of
aching between paroxysms, affecting one of the
more divisions of trigeminal nerve and fulfilling
criteria 2 & 3.
2. Pain has one of the following characteristics
1. Intense, sharp, superficial, stabbing
2. Precipitated from trigger area or trigger factor.
3. Attacks are stereotyped in the individual patient.
4. A causative lesion, other than vascular compression,
has been demonstrated by special investigations and
posterior fossa exploration.
 Clinical characteristics
 Pain arises in the affected person, who
have no abnormal neurological deficit such
as loss of corneal reflex, anesthesia,
parasthesia, muscular atrophy or weakness
 Pain is sudden, unilateral, intermittent
paroxysmal, sharp, shooting, lancinating
shock like pain. Elicited by touching of
superficial trigger points, which radiates to
other branches of trigeminal nerve
 Pain is usually confined to one division and
spreads to adjacent division and rarely
involves all the branches.
 Pain rarely cross the midline.
 Pain is of short duration & lasts for a few
seconds, reoccurs with variable frequency.
Even though there is a refractory period
between the attacks, some patients report a
dull ache in between the attacks.
 Patients with pain will hold the hand over
the face or rub till the pain subsides.
 Males avoid shaving
 Patients will present with a poor oral
hygiene as they avoid brushing the teeth.
 The paroxysms occur in cycles, each cycle lasting for
weeks months and with time the cycles appear closer
& closer with each attack. With each attack the pain
seems to become more intense and unbearable.
 In extreme cases the patients will have a motionless
face – “the frozen of mask like face”.
 The pain triggers on touching the face at a particular
place, chewing, speaking, smiling, brushing, shaving,
washing the face.
 The location of the trigger points depends on which of
trigeminal nerve is involved.
 It is a characteristic of the disorder that attacks do not
occur during sleep.
 Many patients will lead a very poor quality of life.
V2 – skin of the upper lip, ala, nasi, or cheek, or the
upper gums.
V3 – this is the most frequently involved branch.
Lower lip, teeth or gums of the lower jaw. Tongue is
rarely involved.
V1 – the trigger zone usually lie over the supraorbital
ridge of the affected side.
 Its very common for the patients to undergo
indiscriminate dental extraction on the affected side
without any relief from pain, b’coz the pain of the
trigger zone and pain distributions often mimic pain
of odontogenic origin.
 More than 50% of patients experience rarely
remission of greater than 6 months before return of
active pain.
 Diagnosis
 Its mainly from the history
 Symptoms may mimic toothache, sinusitis,
stomatitis or other inflammatory condition.
 Proper clinical examination is necessary.
 The younger age group of patients should alert
the clinician to a possible intracranial space
occupying lesion or intracranial arteriovenous
anomalies. Other D.D. should include sclerosis,
posttherapeutic neuroma or post traumatic
neuralgias
 Imaging
 Imaging studies are indicated b’coz distinguishing between
idiopathic and secondary forms of TN is not always clear.
 CT
 MRI
 Magnetic resonance angiography ( MRA )
 Newer tech: enlarged view
 Conventional angiogram – useful in vascular malformation.
 Clinical neurophysiology testing with a blink reflex
 Selective blocking the nerve ending with LA
 Response to treatment with tablet carbamazepine is
universal in TN, as in other types of facial pain it is not
useful.Many clinician use this response as a step in
definitive diagnosis of the condition.
 Treatment
 Once the diagnosis of trigeminal neuralgia
is established, then the treatment regime
is started first medicinal management is
advocated. If the patient does not respond
to it, then only surgical management is
opted.
 Medical Treatment
 This is the first line approach for most of the
patients.
 TN does not respond to analgesics including
opiates.
 Anticonvulsants – these drugs reduce the firing
potential in the trigeminal nerve.
 Carbamazepine is highly specific in only reliving
pain of TN. The response can be used as an
diagnostic indicator.
 Carbamazepine has a special effect on the
paroxysmal pain. The use of this drug causes
paroxysms to become separate by intervals of
freedom for weeks, months or even years.
This is considered to be the conservative treatment
for trigeminal neuralgia.
As an initial dose 100mg is given twice daily until
relief is established.
At no time the daily dose should exceed 1200mg.
The dose at night is more so that to prevent attack in
the morning as the drug level in the blood is
maintained.
Side effects: dizziness, unsteady gait, GI distress,
skin rashes and aplastic aneamia.
Dosage is reduced by 200mg if side effects appear.
If not controlled then sodium valproate 600mg/day is
added on.
With phenytoin or baclofen also.
Clonazepam is used when carbamazepine is
contraindicated.
 Tab phenytoin – dose: 100mg t.i.d.
 Side effects: slurred speech, abnormal movements,
swelling of the lymph nodes, gingival hypertrophy,
hirsutism, foliate deficiency.
 Tab oxcarbazepine – Dose: 1200mg/day
 Side effects: hyponalraemia, double vision
 Valproic acid – Dose: 600mg/day
 Side effects: irritability tremors, confusion, hepatotoxity,
weight gain.
 Baclofen ( Lioresal ) – 10mg t.i.d. an antispastic
drug.
 Gabapentin ( neurontin )
 Anti inflammatory agents like indomethacin and
short course of the steroids.
 Trichloro ethylene inhalation.
 Surgical treatment
 Peripheral infections:
 Injection of the peripheral nerve with long acting
anesthetic solution: LA to nerve block provides
temporary relief for few hours and help in diagnosis.
 Injection of the nerve with alcohol: 0.5 – 2.5ml of 95%
absolute alcohol can be used to block the peripheral
branches of the trigeminal nerve. The aim is to destroy
selective nerve fibers. Alcohol block produces total
numbness in the region of distribution of the nerve that
was anesthetized. It’s a relatively easy procedure but
the success rate is low since the nerve block is post
ganglionic. Sensation to the nerve may return in few
months time. Alcohol block should not be given
repeatedly. Blocking the gasserian ganglion may be
more effective but is a more hazardous procedure as it
may cause escape to surrounding subarachonoid
space & cause palsy to the adjacent cranial nerves.
Complications: necrosis of the adjacent tissues,
fibrosis and alcohol induced neuritis.
 Peripheral Neurectomy or Nerve avulsion:
 Oldest and the most effective peripheral nerve
destructive technique.
 Simple procedure can be repeated and relatively reliable
technique.
 It acts by interrupting the flow of a significant number of
afferent impulses to central trigeminal apparatus.
 Indicated in patients in whom craniotomy, a more
extensive procedure is contraindicated, b’coz of age,
debility of significant systemic diseases, limited life
expectancy.
 Performed most commonly on infraorbital nerve, mental
nerve, inferior alveolar nerve and rarely lingual nerve.
 Infraorbital neurectomy:
 Incision: the nerve can be approached
conventional intraorally or alternatively by a
braun’s transantral approach.
 Conventional Intraoral approach:
1. A crescent shaped incision is made in the upper buccal
vestibule in the canine fossa region similar to the caldwell –
luc approach and mucoperiostial flap is reflected.
2. The infraorbital foramen and nerve is located.
3. The nerve is held by an artery forceps and the terminal
branches of the nerve are carefully freed from the soft
tissues.
4. The main trunk of the nerve is then carefully held close to
the foramen and twisted slowly around the hemostat and
removed from the foramen.
5. The infraorbital foramen is plugged with poly – ethylene
plug and wound is closed with interrupted sutures.
 Braun’s transantral approach:
1. The key to this approach is a thorough knowledge of anatomy.
2. The nerve can also be approached through the maxillary
antrum.
3. Through this approach, the maxillary nerve can be sectioned.
4. An intraoral incision is placed from the zygomatic buttrees to
the labial frenum and a mucoperiosteal fiap reflected to expose
the entire anterior and lateral wall of the maxillary antrum
5. an opening is made in the anterior wall of the maxillary
antrum, the sinus lining is reflected in the posterior wall.
6. The descending palatine branch of the trigeminal nerve is
identified and traced to the sphenopalatine ganglion.care is
taken to prevent damage to the maxillary artery, posterior
superior alveolar artery.
7. The maxillary nerve is sectioned from the foramen rotundum to
the inferior orbital fissure.
8. The sharp bony edges are smoothened and the flap sutured
bask in position.
 Inferior alveolar nerve neurectomy:
By 2 methods: intraoral approach and extraoral approch
 Intraoral approach is preferred as it is simple and more
cosmetic.
 Extraoral approach - through risdon’s incision
 Intra oral approach – via dr. Ginwalla’s incision
1. It is mainly used in dentulous patients.
2. The incisions extends from the anterior border of the ramus
along the coronoid process up to the retromolar region. From
here the incision splits into two parts, one extending lingully
and the other extending bucally like an inverted ‘y’. Another
incision is made in the region of the first premolar to expose
the mental nerve.
3. The medial aspect of the ramus is exposed and the inferior
alvelora nerve is identified and exposed as superiorly as
possible.
4. The nerve is ligated at two points in the most
superior part visible and divided between the
ligatures. The superior end is cauterized and the
lower end is held securely using a hemostat.
5. The mental nerve is also similarly ligated in two
points close to the mental foramen and divided
between the two.
6. The mental nerve is freed from the surrounding
soft tissues and removed.
7. The remaining nerve is held at the inferior alveolar
end and wounded around the hemostat and
excised from the canal.
8. The wound is closed in layers with interrupted
sutures.
 Lingual neurectomy:
 An incision is made in
the anterior border of
the ramus slightly
towards the lingual side.
 The lingual aspect is
exposed and the lingual
nerve is identified in the
third molar region just
below the periosteum
 The nerve can be either
avulred or cauterized
and cut.
 The wound is closed
with interrupted sutures
 Cryotherapy or Cryoneurolysis for
peripheral nerves.
 Barnard first used cryotherapy in 1081 for the treatment of
TN.
Technique:
 Procedure can be done under LA and sedation
 After identifying the affected nerve with local anesthetic
blocks, the nerve is exposed to the cryoprobe intra orally.
 The nerve is exposed for 2 min freeze followed by 5min
thaw cycle, the freeze thaw cycle is repeated at least 3
times.
 Most patients return with a reoccurance of pain within 48hrs.
 Nitrous oxide cryotherapy is seen to have lower
reoccurance of pain compared to liquid nitrogen therapy.
 Electrocoauglation of gasserian
ganglion
 Diathermy apparatus is placed in the
gasserian ganglion to coagulate and
destroy it.
 Percutaneous radiofrequency
trigeminal neurolysis
 It is a technique in which there is a use of
controlled radiofrequency.
 It is performed by insertion of temperature
monitoring electrode through foramen ovale
into trigeminal ganglion
 The temperature is raised to 60 to 90 degree
Celsius.
 Advantages include decreased mortality and
morbidity and permanent cure.
 Disadvantages include development of painful
anesthesia, keratitis, corneal anesthesia and
sixth cranial nerve palsy
 Decompression and compression:
 Percutaneous micro compression : in this inflated balloon is used to
compress the gasserian ganglion
 Micro vascular decompression – retromastoid craniotomy is used
and the offending vascular structure are dissected free of the nerves
at root entry zone and maintained in that position by insertion of a
small piece of gel , foam of ivalon sponge
 Rhizotomy – actual cutting of trigeminal sensory root results
in permanent anesthesia in most patients. The reoccurrence
rate of trigeminal neuralgia after rhizotomy is 20%.
 Bulbar trigeminal tractotomy – sensory origin of trigeminal
nerve runs from the upper pons through the medulla and in
upper cervical rod. This descending tract of the trigeminal
nerve may be cut in the area of medulla oblongata to induce
loss of pain and temperature sensation with nearly total
retention of proprioception.
 Post operative care
All surgical procedure carry a risk of sensory loss
while this may be inconvenient when affecting
the 2nd and 3rd trigeminal division, anesthesia of
the first division and thus the cornea is
potentially highly dangerous an unrecognized
scaring can lead to blindness. All patients should
therefore have an eye shield applied until they
are co – operative enough for corneal sensation
to be tested. If sensation is absent and fails to
return, special glasses with side panels should
be worn, and the patient instructed about
appropriate eye care.
Routine clinical observations are sufficient for
patients following percutaneous procedures and
they can usually be allowed home the same or
the following day.
 Open procedures carry more serious risks
observations in an intensive care or high
dependence unit is recommended as the
development of a posterior fossa haematoma, is
a life threatening emergency. The patient will
often have headache or be dizzy or nauseated
for a day or two and will not usually be
discharged until the third or fourth postoperative
day.
 If pain is abolished by the procedure, medication
may be withdrawn immediately although some
patients prefer a gradual withdrawal.
 BIBLIOGRAPHY
 ORAL SURGERY,ORAL MEDICINE,ORAL
PATHOLOGY,ORAL RADIOLOGY AND
ENDODONTOLOGY.
NOV 2005 VOL 100 EDITORS; FIRRIOLO AND
THOMAS SOLLECITO.
 TEXT BOOK OF ORAL AND MAXILLOFACIAL
SURGERY
NEELIMA ANIL MALIK.
 TEXT BOOK OF ORAL AND MAXILLOFACIAL
SURGERY
SM BALAJI.
 TEXT BOOK OF ORAL MEDICINE
ANIL GOVINDRAO GHOM.
Thank you.